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USE OF VENOVENOUS EXTRACORPOREAL MEMBRANE OXYGENATION WITHOUT HEPARIN FOR A PATIENT WITH CONCOMITANT INJURY
Skopets A.A., Zharov A.S., Potapov S.I., Afonin E.S., Utegulov M.G., Kozlov D.V., Chibirov S.K., Mukhanov M.L., Shevchenko A.V., Baryshev A.G., Porkhanov V.A.
Research Institute-Ochapovsky Regional Clinical Hospital No.1, Kuban State Medical University, Krasnodar, Russia
Due
to technical progress and accumulated clinical experience, the use of
venovenous extracorporeal membrane oxygenation (vv-ECMO) has become the
therapeutic standard for salvation of lives of patients with acute respiratory
distress syndrome (ARDS) [1-3]. The expert group made a conclusion after a
randomized controlled study (CESAR) of ECMO: it is necessary for severe ARDS [4].
Realization of ECMO requires for a well-trained multi-disciplinary team. Its
realization can lead to serious complications relating to disordered blood flow
in extremities, blood loss etc. Sometimes, ECMO plays a role of a life-saving
procedure, when other methods are non-efficient [5, 6].
Anticoagulation
and hemotransfusion are standard for ECMO to prevent platelet activation and
subsequent catastrophic insufficiency of extracorporeal contour of
thromboembolic complications.
Development
of centrifuge pumps of new generation, and low-resistant polymethylpentene
oxygenerators was directed to a decrease in thrombogenicity of ECMO-contour and
intracontour hemolysis [2, 7]. Anticoagulation by itself does not cause any
hemorrhagic complications, which are common (15-25 %) and can be fatal [1, 3,
10]. Less severe complications in critically ill patients are determined by
anemia and risks relating to high transfusion requirements. High risk of
complications in ECMO in patients with severe concomitant injury stimulates the
interest to minimization of anticoagulation strategy.
Severe
concomitant injury is a cause of death in young people in 55-80 % of cases; a
cause of lethal outcome is often related to lung involvement since injuries to
chest organs are identified in 50 % of patients [11, 12]. Hemorrhagic shock and
post-injury severe respiratory insufficiency are common pacemaker of fatal
complications [13].
Despite
the fact that the first successful use of ECMO was realized in treatment of
posttraumatic ARDS in 1971, this technique for treatment of patients with
severe concomitant injury did not become main due to hemorrhagic complications
[14].
The
literature describes some cases of ECMO use for patients with various injuries,
with some patterns and sometimes poor outcomes [11, 14-19]. The received
results and high risk of bleeding progression do not stimulate the wide use of
ECMO in this population of patients [9]. More detailed studies of data bases
showed that patients with injuries and extracorporeal support demonstrated the
survival rate of 44-74.1 % [10-15], like the previously reported survival of 58
% in general population of adults with respiratory ECMO [16]. Extracorporeal
membrane oxygenation maintains systemic oxygenation of tissues when pulmonary
function is disordered. However it is considered that ECMO is contraindicated
for some patients, especially for ones with risk of bleeding after use of systemic
anticoagulants, for example, in patients with closed chest injuries with
bleeding relating to lung contusion and other organ injuries [8].
Therefore,
it is important to pay attention to the factors, which promote bleeding or
coagulopathy. The use of ECMO without heparin can be a key to salvation of the
problem of systemic oxygenation during treatment. Several cases of ECMO in
patients with massive hemothorax after pulmonary parenchymal injury were
described [10]. In this report, we present a clinical case of successful use of
ECMO without heparin for a female patient (age of 19) with respiratory failure
determined by extensive bilateral lung injury.
Objective – to discuss the possibilities of extracorporeal life support in patients
with trauma profile.
The study was conducted in compliance with World Medical Association Declaration of Helsinki –
Ethical Principles for Medical Research Involving Human Subjects, 2013, and the
Rules for Clinical Practice in the Russian Federation (the Order by Healthcare
Ministry of Russia, June 19, 2003, No.266), with the written consent for
participation in the study and for use of personal data.
MATERIALS AND METHODS
The
patient, age of 19, was admitted on September 26, 2019, on the fourth day after
a road traffic accident. The diagnosis was: "Concomitant injury to the
head, the chest, the spine, the pelvis and extremities; contused wounds of the
face; a closed chest injury; lung contusion; pneumomediastinum; closed
fractures of ribs 1-5 to the right and rib 2 to the left; a closed fracture of middle
one-third of both bones of the right leg with displaced fragments; a lineal
fracture of anterior arch of C1 without displaced fragments; a fracture of
transverse processes of Th1, Th3-7 without displacement of fragments to the
right".
In
the level 2 trauma center (central regional hospital), the fracture of leg
bones was fixed with external fixation apparatus. Due to progression of
respiratory failure, a decision was made to transfer the patient to the level 1
trauma center (regional clinical hospital). The patient was transported by an ambulance
car. Her condition was very severe, and was conditioned by the concomitant
injury, severe respiratory failure, unstable hemodynamics and metabolic
disorders. Skin surface was edematous, pale cyanotic. There were some scratches
on her right cheek, nose, right and left ankles, and on the dorsal surface of
the left foot.
The
patient was in condition of drug sedation (consciousness was clear without
sedation; psychomotor agitation was +2 according to RASS). Artificial lung
ventilation was conducted with Drager Evita-4 with SIMV mode; ventilation
parameters: Vt – 550 ml, f – 14/min, FiO2 –
80-100 %, Рреак
35 cm H2O, PEEP 14 cm H2O. Vesicular breathing was weak.
There were some moist rales.
SpO2 –
45-60 %. Hemodynamics was unstable. Infusion of noradrenaline - 0.1-0.3
µg/kg/min, AP - 100-115/55-79 mm Hg, HR - 95-110 min, sinus rhythm.
Note:
SIMV - synchronized intermittent mandatory ventilation, Vt - tidal volume (ml),
f – respiratory rate, FiO2 - oxygenation index, Рреак
– peak flow value, PEEP - positive end-expiratory pressure, SpO2 –
blood oxygen saturation.
Fibrobronchoscopy showed
bilateral diffuse catarrhal endobronchitis with mucous hemorrhagic secretion.
A study of arterial
blood gases: pH – 7.31, PaCO2
– 42.4 mm Hg, PaО2 – 50.6 mm Hg, Hb – 77
g/l, SаO2
– 76.6 %, BE – 1.6
mmol/l, HCO3 – 21.2 mmol/l,
К+ – 3.51 mmol/l, Na+ – 138.4 mmol/l, glucose – 5.8
mmol/l, lactate – 4.61 mmol/l.
Leg fractures were fixed with
external apparatus.
The patient had severe respiratory
insufficiency, ARDS infiltration in four quadrants, РаО2/FiO2
– 128, Рреак
– 35 cm H2O, PEEP – 17 cm H2O, compliance - 39 ml/cm H2O,
Murrey index - 3.5. A decision on initiation of vv-ECMO was made owing to
progressing respiratory failure, despite of high risk of hemorrhagic
complications at the background of systemic heparinization.
On September 27, 2019, at
11:35 a.m., cannulation of the right femoral artery and the right internal
jugular vein was performed under X-ray control in the catheterization
laboratory. Cannulas 17Fr and 19Fr were installed. Venovenous extracorporeal
membrane oxygenation was initiated (the scheme - right femoral vein - right
internal jugular vein) with perfusion rate of 5-6.5 l/min/m2, V – 4 l/min, DO2 – 100 %. Systemic
anticoagulation was conducted only before cannulation with single-stage
intravenous introduction of 2,500 units of heparin. The same dose of heparin was added to primary
volume of ECMO-contour. Activated clotting time before cannulation was 158 sec.
ALV was continued with
BiPAP with parameters: FiO2 – 50 %, f – 16/min, Pinsp – 17 cm H2O,
PEEP – 5 cm H2O.
Note:
BiPAP – ventilation mode at two levels of CPAP with switching between pressure
levels through targeted time intervals, Vt - tidal volume (ml), f – respiratory
rate, FiO2 - oxygenation index, Pinsp – high pressure phase, PEEP
-positive end-expiratory pressure, DO2 – percentage of oxygen
delivered to mixer of ECMO device.
Arterial blood gases:
pH – 7.37; PaCO2 – 41.8 mm Hg; PaО2 – 59 mm Hg, Hb – 95
g/l; SO2 – 83.4 %; К+ – 3.5 mmol/l; Na+ – 136
mmol/l; glucose – 6.8 mmol/l; lactate – 3.65 mmol/l; BE – 1.6
mmol/l; HCO3 – 23.0 mmol/l.
Echocardiography showed ejection
fraction (EF) > 55 %, tricuspid regurgitation 2-3+, pulmonary hypertension
(systolic pressure in pulmonary artery - 50-60 mm Hg).
Computer imaging (CI) of chest
organs identified some negative time trends of bilateral infiltrative process
in the lungs, and pneumomediastinum. There were fractures of ribs 1-5 to the
right, and rib 2 to the left, fractures of transverse processes Th1 and Th3-7
to the right.
Extracorporeal respiratory support
with vv-ECMO was conducted within 6 days. Within the whole period of vv-ECMO,
volumetric rate of perfusion was within 4.5-5 l/min, with rotation rate of the
centrifuge pump of 4,000-5,000 r.p.m. Oxygenation was controlled with
monitoring of gas composition of arterial and venous blood, pulse oximetry, and
oximetry with near-infared strectroscopy (NIRS) on the right forearm, right and
left legs. It allowed estimating the oxygenation of the whole body, and
peripheral perfusion of the extremity with the cannula. Left leg NIRS was rSO2 – 68-65 %, for the right leg - 38-41 %, for the right
forearm - rSO2 – 70-67 %. The cause of decreasing oxygenation in the right leg
was edema after a fracture of the middle one-third of both bones of the right
leg with displacement of fragments.
The time course of
changes in gas composition of arterial blood is presented in the table 1.
Table 1. Time course of arterial and venous blood gases during VV-ECMO
|
Value |
At admission |
Before ECMO |
day 1 of ECMO |
day 2 of ECMO |
day 3 of ECMO |
day 4 of ECMO |
day 5 of ECMO |
day 6 of ECMO |
Before weaning from ECMO |
day 1 after ECMO |
day 2 after ECMO |
|
26.09.19 |
27.09.19 |
27.10.19 |
28.10.19 |
29.10.19 |
30.10.19 |
01.11.19 |
02.11.19 |
03.11.19 |
04.11.19 |
05.11.19 |
|
|
Artery |
|||||||||||
|
FiO2 |
0.8 |
1.0 |
0.5 |
0.5 |
0.35 |
0.5 |
0.5 |
0.5 |
0.5 |
0.3 |
0.3 |
|
pH |
7.31 |
7.41 |
7.37 |
7.52 |
7.47 |
7.42 |
7.42 |
7.47 |
7.43 |
7.51 |
7.46 |
|
PaCO2 |
42.40 |
38.50 |
41.80 |
32.90 |
34.80 |
37.10 |
40.00 |
33.90 |
36.50 |
33.00 |
34.10 |
|
PaO2 |
50.60 |
128.90 |
58.80 |
81.30 |
84.00 |
73.60 |
97.80 |
81.60 |
98.50 |
165.00 |
92.10 |
|
Hb |
77.00 |
91.00 |
95.00 |
103.00 |
156.00 |
174.00 |
155.00 |
136.00 |
100.00 |
177.00 |
163.00 |
|
SO2 |
76.60 |
98.60 |
83.20 |
95.40 |
95.90 |
91.50 |
97.10 |
96.30 |
97.30 |
99.20 |
96.70 |
|
K+ |
3.51 |
3.98 |
3.48 |
2.61 |
3.58 |
4.00 |
4.17 |
3.90 |
4.10 |
3.49 |
3.55 |
|
Na+ |
138.40 |
140.00 |
135.70 |
137.00 |
137.10 |
135.00 |
135.50 |
137.00 |
138.00 |
133.60 |
132.30 |
|
Glucose |
5.80 |
4.30 |
6.80 |
5.60 |
5.50 |
5.00 |
5.40 |
5.50 |
6.90 |
6.50 |
5.20 |
|
Lactate |
4.61 |
2.06 |
3.65 |
2.81 |
2.10 |
1.80 |
1.71 |
1.60 |
1.30 |
1.90 |
1.30 |
|
BE |
-4.90 |
-0.40 |
-1.60 |
4.00 |
1.80 |
-0.10 |
1.40 |
1.20 |
0.50 |
3.10 |
0.10 |
|
HCO3- |
20.40 |
24.10 |
23.00 |
28.10 |
26.40 |
24.50 |
25.70 |
25.96 |
25.10 |
27.90 |
25.20 |
|
Vein |
|||||||||||
|
pH |
6.99 |
- |
7.41 |
7.53 |
7.46 |
7.39 |
7.36 |
- |
- |
- |
- |
|
PvCO2 |
53.00 |
- |
36.60 |
31.70 |
38.50 |
44.40 |
52.70 |
- |
- |
- |
- |
|
PvO2 |
30.10 |
- |
43.80 |
67.60 |
42.80 |
46.30 |
36.00 |
- |
- |
- |
- |
|
SvO2 |
20.90 |
- |
66.20 |
92.20 |
67.00 |
68.80 |
46.20 |
- |
- |
- |
- |
|
Lactate |
9.10 |
- |
3.27 |
2.70 |
1.94 |
1.93 |
1.66 |
- |
- |
- |
- |
|
BЕ |
-16.80 |
- |
-1.60 |
3.60 |
3.60 |
1.30 |
4.30 |
- |
- |
- |
- |
|
HCO3- |
10.40 |
- |
22.90 |
27.80 |
27.00 |
24.60 |
26.60 |
- |
- |
- |
- |
Note: pH – acid-alkali balance of blood, PaCO2 – arterial blood carbon dioxide partial pressure, Hb – hemoglobin level, SO2 – oxygen saturation of arterial blood, BE – deficiency or excess of bases for whole extracellular fluid, including blood, PvCO2 – carbon dioxide partial pressure of venous blood, PvO2 – oxygen partial pressure of venous blood.
Systemic heparinization
was not conducted. However, clexane (40 mg, subcutaneously, 2 times per day)
was prescribed. Owing to slight bleeding around the outflow cannula, clexane
was cancelled on the next day, and prescribed again after weaning from ECMO.
Monitoring of
hemoglobin, hematocrit, platelets, blood clotting, antithrombin III, D-dimers,
activated clotting time and free hemoglobin was performed each day. These values are presented in the figure 1-4.
Figure 1. Time course of changes
in values of coagulogram during VV-ECMO
Note: PTT (sec.) – prothrombin time, INR – international normalised ratio, APTT (sec.) – activated partial thromboplastin time, AT III (%) – antithrombin III activity.
Figure 2. Time course of changes
in hemoglobin, hematocrit and platelets during VV-ECMO
Figure 3. Time course of changes
in D-dimer during VV-ECMO
Figure 4. Time course of changes in
activated coagulation time during VV-ECMO
Analgesia and sedation
were performed by means of continuous infusion of phentanyl (1.5-0.5 µg/kg/h).
Due to need for daily bronchoscopy and activation of the patient, on the third
day of vv-ECMO, she received transcutaneous dilatation tracheostomy. Owing to
gastric stasis and ischemic hypoxic enterocolitis, the patient received
parenteral nutrition. On the 4th day of ECMO, the intestinal probe was
installed through endoscopic approach, and enteral nutrition was initiated.
The trigger level of
hemoglobin in vv-ECMO was determined by us as 12 g/l. During extracorporeal
membrane respiratory support without heparin infusion, the patient received 12
doses of packed red blood cells, and 26 doses of fresh-frozen plasma (FFP).
The table 2 presents the
data on transfusion of blood components.
Table 2. Transfusion of blood components during VV-ECMO
|
Blood components |
26.09.19 |
27.09.19 |
27.09.19 |
28.09.19 |
29.09.19 |
30.09.19 |
1.10.19 |
2.10.19 |
3.10.19 |
|
Erythrocytic suspension, ml |
373 |
353 |
323 |
- |
323 |
- |
- |
333 |
303 |
|
353 |
- |
353 |
- |
303 |
- |
- |
- |
353 |
|
|
- |
- |
333 |
- |
- |
- |
- |
- |
- |
|
|
Total (erythrocytic suspension) |
726 |
353 |
1009 |
0 |
626 |
0 |
0 |
333 |
656 |
|
Fresh frozen plasma (FFP), ml |
280 |
300 |
600 |
210 |
- |
600 |
- |
600 |
- |
|
290 |
280 |
600 |
600 |
- |
600 |
- |
600 |
- |
|
|
- |
- |
600 |
600 |
- |
- |
- |
- |
- |
|
|
- |
- |
280 |
300 |
- |
- |
- |
- |
- |
|
|
- |
- |
- |
220 |
- |
- |
- |
- |
- |
|
|
Total (FFP) |
570 |
580 |
2080 |
1930 |
0 |
1200 |
0 |
1200 |
- |
The changes in time course of inflammatory-infiltrative process in the lungs was controlled with recurrent computer imaging of the chest organs. The first examination after transfer from the central regional hospital showed some regions of low airiness by type of "ground glass" which interfused and were more apparent in the lower parts. On the second day after initiation of ECMO, the increase in intensity and incidence of changes in lung parenchyma was found (Fig. 5-7).
Figure 5. Patient, age of 19. Thoracic CT before VV-ECMO
Figure 6. Patient, age of 19.
Thoracic CT before VV-ECMO
Figure 7. Patient, age of 19. Thoracic CT before VV-ECMO
On the 5th day of ECMO, chest CI showed some positive trends in bilateral infiltrative process in the lungs (possibly, ARDS) (Fig. 8-10).
Figure 8. Patient, age of 19. Thoracic CT during VV-ECMO
Figure 9. Patient, age of 19.
Thoracic CT during VV-ECMO
Figure 10. Patient, age of 19. Thoracic CT during VV-ECMO
At the moment of admission, the bronchoscopic study showed pale pink mucosa with hemorrhage; the vascular pattern was blurred. There was a moderate amount of mucous hemorrhagic secretion in the lumen of bronchi of the lower lobes. During videobronchoscopy, which was performed for transcutaneous puncture tracheostomy four days later, the right and left-sided bronchial mucosa was moderately edematous, with hyperemia. The vascular pattern was not visible. There was a moderate amount of cloudy mucous purulent secretion.
RESULTS
On the sixth day after a
successful test with cancellation of oxygen-air mixture to ECMO-contour, the
patient was weaned from ECMO.
The components of
ECMO-contour were properly studied. There were not any clots and thrombotic
deposits on the walls of the oxygenator, on the centrifuge pump and on the
trunks (Fig. 11-13).
Figure 11. Contour after VV-ECMO
without heparin
Figure 12. Centrifugal pump after
VV-ECMO without heparin
Figure 13. Oxygenator after VV-ECMO
without heparin
On the next day after weaning from ECMO, the tracheostomy tube was removed, and high-flow oxygen therapy with FiO2 of 30 % was initiated. On the fourth day after weaning from ECMO, osteosynthesis was carried out. On the seventh day after surgery, the patient's condition was satisfactory, and she was transferred to the hospital according to her place of residence.
DISCUSSION
We described the case of
severe closed injury, which required for ECMO without heparin due to massive
hemorrhage after a road traffic accident. We can find a lot of reports on ECMO
without heparin in severe closed injury to the chest, but all of them present
retrospective, observational or cohort studies [11, 14-19], and presentations
of case histories are rare [9, 10]. Therefore, we described the detailed report
on a severe blunt chest injury with CT images of the chest, bronchoscopy and
laboratory data.
Annually, approximately
5 million of deaths are caused by severe trauma [13, 27]. A lot of patients
well response to special techniques of trauma management, including infusion
therapy, ALV and other invasive procedures. However patients with simultaneous
severe chest trauma and hemorrhagic shock show quite poor prognosis. The main
aims of management of patients with severe closed chest trauma and hemorrhagic
shock are recovery of blood clotting by means of transfusion of blood
components (erythrocytes, platelets, fresh frozen plasma), surgical arrest of
bleeding, and maintenance of body temperature [15, 16]. It is considered that
in absence of bleeding from organs except for lungs, the use of ECMO will
possibly cause the low risk of additional hemorrhagic problems [34]. However in
presence of bleedings from other injuries, ECMO should be considered with
caution, depending on possibility of control of any additional source of hemorrhage. Early initiation of ECMO has a
possible risk of ECMO-associated complications in trauma patients, especially
with hemorrhage. Trauma-induced coagulopathy is a well-described process
relating to significant values of morbidity and mortality [28-31]. Bleedings
cause serious problems for treatment of trauma patients. Hemorrhagic
complications are registered in 35-59 % of patients with ECMO [17, 19]. In
attempts of minimizing risk of bleeding in patients with ECMO in the
posttraumatic period, some special strategies of management were described,
such as ECMO without heparin, and titration of activated clotting time (ACT)
[13, 17, 18].
Within the last decades,
some technical advances in ECMO such as heparin-coated contours, and
polymethylpentene oxygenerators decreased the thrombogenic potential, and, as
result, softened the demands for anticoagulopathy [32]. These technical
advances allowed individualization of estimation of bleeding and subsequent
changes in anticoagulation parameters in trauma patients, with use of minimally
possible anticoagulopathy when required [13, 18]. ECMO without heparin is also considered
for such patients. In similar manner, if active bleeding from bronchi is
identified (also bleeding after lung contusion), the possibility of control of
these hemorrhage sources should be considered in initiation of ECMO regardless
of bleedings from other organs. It is considered that ECMO without heparin is
appropriate for trauma patients, despite of worse survival [20]. Therefore, for
prevention of thrombosis and clotting, we focused on blood flow intensity in
ECMO. In our case, for prevention of thrombosis, considering the possibility of
clot formation in use of ECMO without heparin, for "the rest" of
lungs, we installed the flow at higher rate than usual blood flow in ECMO. In
this period, it is very important to check the values of blood clotting, ACT,
APTT, prothrombin and D-dimers. D-dimer is the very sensitive marker of blood
clotting. In our case, as we expected, the level of D-dimer was gradually
decreasing as compared to the basic level (determined by posttraumatic
hematoma). Therefore, there were not any complications relating to clot
formation during vv-ECMO. Immediately before weaning from vv-ECMO, the level of
D-dimer increased above the basic level.
Therefore, considering
the use of ECMO for improvement in oxygenation in patients with severe injury,
and bleeding, which is difficult to control, it is recommended: 1) single bolus
of small dose of heparin (2,500 units) before vascular cannulation, and the
same dose for primary volume of pump contour; 2) higher rates of blood flow as
compared to recommended rates for non-trauma patients, to prevent thrombosis in
ECMO-contour. It is the new and important information on treatment of severe
concomitant injury.
Damage control focuses
on rapid arrest of bleeding and on stabilization of main vital functions
-breathing and blood circulation. Arlt et al. reported that use of heparinless
ECMO is appropriate for survival of patients with closed injury, respiratory
failure and hemorrhagic shock [13]. Despite of contraindications, for patients
with closed trauma and hemorrhagic shock, surgical correction with subsequent
ECMO can be realized if bleeding is well controlled. In this case, we used ECMO
since the patients had no irreversible injuries, and bleeding control was
adequate after fixation of the main fractures. The results of computer imaging
did not identify any ALV-related barotrauma or hemorrhage-related
complications.
From other side, long
term heparinless ECMO was successfully used for patients with severe traumatic
brain injury (TBI) [21, 33]. It is possible that higher frequency of TBI will
show independent correlation with worse results in patients with ECMO and
traumatic respiratory insufficiency.
We think that further
use of heparin makes the clinically significant influence, and further studies
are required for identification of this influence, especially in patients with
TBI.
Therefore, ECMO has some
degree of risk for patients with serious trauma. So, ECMO can be the first line
of therapy in patients with traumatic lung contusion, ARDS and alveolar
bleeding, and its use is disputable for patients with injuries and bleeding.
However for patients
with severe traumatic lung injury and alveolar bleeding with hard-to-treat
hypoxemia and hypercapnia, the use of ECMO can be a key to survival in such
situation.
CONCLUSION
ECMO can be an additional technique for treatment of adult patients with severe closed lung injury or acute respiratory failure resistant to standard ventilation. With appropriate observation, ECMO can be the safe and efficient technique for life salvation in patients with severe chest trauma and concurrent hemorrhagic shock.
Information on financing and conflict of interest
The
study was conducted without sponsorship.
The
authors declare the absence of any clear and potential conflicts of interests
relating to publication of this article.
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